scholarly journals Bioinformatic analysis of key pathways and genes involved in pediatric atopic dermatitis

2020 ◽  
Author(s):  
Tianyi Wang ◽  
Bingxin Zhang ◽  
Danhui Li ◽  
Xiaoli Qi ◽  
Chijin Zhang
Keyword(s):  
Atopic Dermatitis ◽  
Actin Cytoskeleton ◽  
Signaling Pathway ◽  
Expression Profiles ◽  
Receptor Interaction ◽  
Interleukin 17 ◽  
Hub Genes ◽  
Chemokine Signaling ◽  
Chemokine Signaling Pathway ◽  
Regulation Of Actin Cytoskeleton

The initiation of atopic dermatitis (AD) typically happens very early in life, but most of our understanding of AD is derived from studies on AD patients in adult. The aim of this study was to identify gene signature speficic to pediatric AD comapred to adult AD. The gene expression profiles of four datasets (GSE32924, GSE36842, GSE58558, and GSE107361) were downloaded from the GEO database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) enrichment analyses were performed, and protein-protein interaction (PPI) network was constructed by Cytoscape software. Total 654 differentially expressed genes (DEGs) (394 up-regulated and 260 down-regulated) were identified in pediatric AD samples with adult AD samples as control. The up-regulated DEGs were significantly enriched in the migration and chemotaxis of granulocyte and neutrophil, while down-regulated DEGs were significantly enriched in biological adhesion. KEGG pathway analysis showed that up-regulated DEGs participated in chemokine signaling pathway while down-regulated DEGs participated in adherens junction, Focal adhesion, Regulation of actin cytoskeleton. The top 10 hub genes, GAPDH, EGFR, ACTB, ESR1, CDK1, CXCL8, CD44, KRAS, PTGS2, SMC3 were involved in chemokine signaling pathway, cytokine-cytokine receptor interaction, interleukin-17 signaling pathway, and regulation of actin cytoskeleton. In conclusion, we identified DEGs and hub genes involved in pediatric AD, which might be used as therapeutic targets and diagnostic biomarkers for pediatric AD.

scholarly journals Investigation of Potential Genetic Biomarkers and Molecular Mechanism of Ulcerative Colitis Utilizing Bioinformatics Analysis

2019 ◽  
Author(s):  
Jiaqi Zhang ◽  
Xue Wang ◽  
Lin Xu ◽  
Zedan Zhang ◽  
Fengyun Wang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Gene Therapy ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Functional Enrichment ◽  
Hub Genes ◽  
Amyloid A ◽  
Chemokine Signaling ◽  
Chemokine Signaling Pathway ◽  
Potential Biomarkers

Abstract Objectives: To reveal the molecular mechanisms of ulcerative colitis (UC) and provide potential biomarkers for UC gene therapy. Methods: We downloaded the GSE87473 microarray dataset from the Gene Expression Omnibus (GEO) and identified the differentially expressed genes (DEGs) between UC samples and normal samples. Then ,a module partition analysis was performed based on a weighted gene co-expression network analysis (WGCNA),followed by pathway and functional enrichment analyses. Furthermore, we investigated the hub genes . At last, data validation was performed to ensure the reliability of the hub genes. Results: Between UC group and normal group, 988 DEGs were investigated . The DEGs were clustered into 5 modules using WGCNA. These DEGs were mainly enriched in functions such as the immune response, the inflammatory response and chemotaxis, and they were mainly enriched in KEGG pathways such as the cytokine-cytokine receptor interaction , chemokine signaling pathway, and complement and coagulation cascades. The hub genes, including dual oxidase maturation factor 2(DUOXA2), serum amyloid A (SAA) 1 and SAA2, TNFAIP3-interacting protein 3(TNIP3), C-X-C motif chemokine (CXCL1), solute carrier family 6 member 14(SLC6A14) and complement decay-accelerating factor (CD antigen CD55),were revealed as potential tissue biomarkers for UC diagnosis or treatment. Conclusions: This study provides supportive evidence that DUOXA2, A-SAA, TNIP3, CXCL1, SLC6A14 and CD55 might be used as potential biomarkers for tissue biopsy of UC, especially SLC6A14 and CD55, which may be new targets for UC gene therapy. Moreover, the DUOX2/DUOXA2, NF-κB /TNIP3 and CXCL1/CXCR2 pathways might play an important role in the progression of UC through the chemokine signaling pathway and inflammatory response.

scholarly journals Mammary Transcriptome Profile during Peak and Late Lactation Reveals Differentially Expression Genes Related to Inflammation and Immunity in Chinese Holstein

Animals ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 510
Author(s):  
Ziyin Han ◽  
Yongliang Fan ◽  
Zhangping Yang ◽  
Juan J. Loor ◽  
Yi Yang
Keyword(s):  
Mammary Gland ◽  
Signaling Pathway ◽  
Receptor Interaction ◽  
Gene Expressions ◽  
Chinese Holstein ◽  
Chemokine Signaling ◽  
Transcriptomic Sequencing ◽  
Receptor Signaling Pathway ◽  
Differential Expressed Genes ◽  
Chemokine Signaling Pathway

Somatic cell count (SCC) in milk is widely used in the dairy industry, as an indicator of the health of mammary gland. While the SCC of dairy cattle was higher in late lactation than in peak lactation, its association with gene expressions of mammary gland were largely unknown. In this study, a transcriptomic sequencing approach and bioinformatics analysis were used to investigate the differential expressed genes (DEGs) associated with inflammation and immunity between peak and late periods of lactation in Chinese Holstein. A total of 446 DEGs (padj < 0.05 and fold change >2) were identified, 50 of which belonged to seven pathways and five terms related to inflammation and immunity. Our data suggested that the activation of nuclear transcription factor-κB (NF-κB) pathway and Toll-like receptor signaling pathway caused inflammatory response, and the activation of chemokine signaling pathway and cytokine–cytokine receptor interaction signaling pathway caused a protective immune response to ensure dairy cows health during late lactation. Our findings deepen the understanding of the molecular mechanism and physiological functions of mammary inflammation in Chinese Holstein during late lactation.

scholarly journals Investigation of Potential Genetic Biomarkers and Molecular Mechanism of Ulcerative Colitis Utilizing Bioinformatics Analysis

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Jiaqi Zhang ◽  
Xue Wang ◽  
Lin Xu ◽  
Zedan Zhang ◽  
Fengyun Wang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Gene Therapy ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Functional Enrichment ◽  
Hub Genes ◽  
Amyloid A ◽  
Chemokine Signaling ◽  
Chemokine Signaling Pathway ◽  
Potential Biomarkers

Objectives. To reveal the molecular mechanisms of ulcerative colitis (UC) and provide potential biomarkers for UC gene therapy. Methods. We downloaded the GSE87473 microarray dataset from the Gene Expression Omnibus (GEO) and identified the differentially expressed genes (DEGs) between UC samples and normal samples. Then, a module partition analysis was performed based on a weighted gene coexpression network analysis (WGCNA), followed by pathway and functional enrichment analyses. Furthermore, we investigated the hub genes. At last, data validation was performed to ensure the reliability of the hub genes. Results. Between the UC group and normal group, 988 DEGs were investigated. The DEGs were clustered into 5 modules using WGCNA. These DEGs were mainly enriched in functions such as the immune response, the inflammatory response, and chemotaxis, and they were mainly enriched in KEGG pathways such as the cytokine-cytokine receptor interaction, chemokine signaling pathway, and complement and coagulation cascades. The hub genes, including dual oxidase maturation factor 2 (DUOXA2), serum amyloid A (SAA) 1 and SAA2, TNFAIP3-interacting protein 3 (TNIP3), C-X-C motif chemokine (CXCL1), solute carrier family 6 member 14 (SLC6A14), and complement decay-accelerating factor (CD antigen CD55), were revealed as potential tissue biomarkers for UC diagnosis or treatment. Conclusions. This study provides supportive evidence that DUOXA2, A-SAA, TNIP3, CXCL1, SLC6A14, and CD55 might be used as potential biomarkers for tissue biopsy of UC, especially SLC6A14 and DUOXA2, which may be new targets for UC gene therapy. Moreover, the DUOX2/DUOXA2 and CXCL1/CXCR2 pathways might play an important role in the progression of UC through the chemokine signaling pathway and inflammatory response.

scholarly journals Analysis of Potential Genes and Pathways Involved in the Pathogenesis of Acne by Bioinformatics

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Biao Chen ◽  
Yan Zheng ◽  
Yanhua Liang
Keyword(s):  
Signaling Pathway ◽  
Normal Skin ◽  
Enrichment Analysis ◽  
Bioinformatic Analysis ◽  
Cytokine Receptor ◽  
Receptor Interaction ◽  
Ppi Network ◽  
Pathway Enrichment ◽  
Chemokine Signaling ◽  
Chemokine Signaling Pathway

Acne is the eighth most frequent disease worldwide. Inflammatory response runs through all stages of acne. It is complicated and is involved in innate and adaptive immunity. This study aimed to explore the candidate genes and their relative signaling pathways in inflammatory acne using data mining analysis. Microarray data GSE6475 and GSE53795, including 18 acne lesion tissues and 18 matched normal skin tissues, were obtained. Differentially expressed genes (DEGs) were filtered and subjected to functional and pathway enrichment analyses. Protein–protein interaction (PPI) network and module analyses were also performed based on the DEGs. In this work, 154 common DEGs, including 145 upregulated and 9 downregulated, were obtained from two microarray profiles. Gene Ontology and pathway enrichment of DEGs were clustered using significant enrichment analysis. A PPI network containing 110 nodes/DEGs was constructed, and 31 hub genes were obtained. Four modules in the PPI network, which mainly participated in chemokine signaling pathway, cytokine–cytokine receptor interaction, and Fc gamma R-mediated phagocytosis, were extracted. In conclusion, aberrant DEGs and pathways involved in acne pathogenesis were identified using bioinformatic analysis. The DEGs included FPR2, ITGB2, CXCL8, C3AR1, CXCL1, FCER1G, LILRB2, PTPRC, SAA1, CCR2, ICAM1, and FPR1, and the pathways included chemokine signaling pathway, cytokine–cytokine receptor interaction, and Fc gamma R-mediated phagocytosis. This study could serve as a basis for further understanding the pathogenesis and potential therapeutic targets of inflammatory acne.

scholarly journals Network-Based Association Study of Obesity and Type 2 Diabetes with Gene Expression Profiles

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Siyi Zhang ◽  
Bo Wang ◽  
Jingsong Shi ◽  
Jing Li
Keyword(s):  
Type 2 Diabetes ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Cell Receptor ◽  
Mapk Signaling ◽  
Chemokine Signaling ◽  
Chemokine Signaling Pathway

The increased prevalence of obesity and type 2 diabetes (T2D) has become an important factor affecting the health of the human. Obesity is commonly considered as a major risk factor for the development of T2D. However, the molecular mechanisms of the disease relations are not well discovered yet. In this study, the combination of multiple differential expression profiles and a comprehensive biological network of obesity and T2D allowed us to identify and compare the disease-responsive active modules and subclusters. The results demonstrated that the connection between obesity and T2D mainly relied on several pathways involved in the digestive metabolism, immunization, and signal transduction, such as adipocytokine, chemokine signaling pathway, T cell receptor signaling pathway, and MAPK signaling pathways. The relationships of almost all of these pathways with obesity and T2D have been verified by the previous reports individually. We also found that the different parts in the same pathway are activated in obesity and T2D. The association of cancer, obesity, and T2D was identified too here. As a conclusion, our network-based method not only gives better support for the close connection between obesity and T2D, but also provides a systemic view in understanding the molecular functions underneath the links. It should be helpful in the development of new therapies for obesity, T2D, and the associated diseases.

scholarly journals Identification of novel biomarkers and candidate small molecule drugs in rheumatoid arthritis and osteoarthritis based on bioinformatics analysis of high-throughput data

2020 ◽  
Vol 40 (12) ◽  
Author(s):  
Bin Zuo ◽  
JunFeng Zhu ◽  
Fei Xiao ◽  
ChengLong Wang ◽  
Yun Shen ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Gene Expression ◽  
Signaling Pathway ◽  
Small Molecule ◽  
Gene Expression Omnibus ◽  
Hub Genes ◽  
Protein Protein Interaction ◽  
Chemokine Signaling ◽  
Limma Package ◽  
Chemokine Signaling Pathway

Abstract Background: Rheumatoid arthritis (RA) and osteoarthritis (OA) are two major types of joint diseases. The present study aimed to identify hub genes involved in the pathogenesis and further explore the potential treatment targets of RA and OA. Methods: The gene expression profile of GSE12021 was downloaded from Gene Expression Omnibus (GEO). Total 31 samples (12 RA, 10 OA and 9 NC samples) were used. The differentially expressed genes (DEGs) in RA versus NC, OA versus NC and RA versus OA groups were screened using limma package. We also verified the DEGs in GSE55235 and GSE100786. Functional annotation and protein–protein interaction (PPI) network construction of OA- and RA-specific DEGs were performed. Finally, the candidate small molecules as potential drugs to treat RA and OA were predicted in CMap database. Results: 165 up-regulated and 163 down-regulated DEGs between RA and NC samples, 73 up-regulated and 293 down-regulated DEGs between OA and NC samples, 92 up-regulated and 98 down-regulated DEGs between RA and OA samples were identified. Immune response and TNF signaling pathway were significantly enriched pathways for RA- and OA-specific DEGs, respectively. The hub genes were mainly associated with ‘Primary immunodeficiency’ (RA vs. NC group), ‘Ribosome’ (OA vs. NC group), and ‘Chemokine signaling pathway’ (RA vs. OA group). Arecoline and Cefamandole were the most promising small molecule to reverse the RA and OA gene expression. Conclusion: Our findings suggest new insights into the underlying pathogenesis of RA and OA, which may improve the diagnosis and treatment of these intractable chronic diseases.

scholarly journals Bioinformatics Analysis of Potential Therapeutic Targets and Prognostic Biomarkers amid CXC Chemokines in Ovarian Carcinoma Microenvironment

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Yunfeng Jin ◽  
Qiwang Lin ◽  
He Fei ◽  
Lujie Xue ◽  
Li Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Ovarian Tissue ◽  
Receptor Interaction ◽  
Biological Regulation ◽  
Downstream Signaling ◽  
Kaplan Meier ◽  
Chemokine Signaling ◽  
Study Results ◽  
Chemokine Signaling Pathway ◽  
Kaplan Meier Plotter

Background. Ovarian cancer (OC) is one of the leading lethal gynecologic cancers of women around the world. More than 70% of patients are diagnosed with stage III or IV with poor outcome. This is partly because of lacking early effective screening techniques and potential biomarkers of OC. CXC chemokines in tumor microenvironment (TME) and their interaction with relative receptors can excite the downstream signaling pathways to influence tumor progression. However, the role of CXC chemokines in OC has not been identified. Methods. ONCOMINE, GEPIA, Kaplan–Meier plotter, cBioPortal, TIMER, Metascape, and LinkedOmics were applied in our study. Results. The transcriptional levels of CXCL1/8/9/10/11/12/13/14/16/17 were significantly elevated while CXCL3 was obviously reduced in OC vs normal ovarian tissue. CXCL8/9/11/13 were correlated with clinic pathological stage. Patients with low expression of CXCL8/9/11/13 were associated with better prognosis. We also found that CXCL3 and CXC12 could be used as potential prognostic markers of OC through Kaplan–Meier plotter. Patients with high expression of CXCL3/12 had a significantly better prognosis. Their functions focus on locomotion, signaling, response to stimulus, undergoing the process of multiorganism, immune system, biological regulation, etc. The differentiated CXC chemokines mainly participate in cytokine-cytokine receptor interaction, chemokine signaling pathway, IL-17 signaling pathway, and toll-like receptor signaling pathway. Our results showed that CXC chemokines were highly correlated with infiltration of immune cells. The kinase targets of differentially expressed CXC chemokines are mainly in ATM, LYN, LCK, PLK1, FYN, CDK2, and ATR. Conclusions. Our results may provide a new insight for selecting precision biomarkers of targeted therapy of OC.

scholarly journals Transcriptome profiling of the diaphragm in a controlled mechanical ventilation model reveals key genes involved in ventilator-induced diaphragmatic dysfunction

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Ruining Liu ◽  
Gang Li ◽  
Haoli Ma ◽  
Xianlong Zhou ◽  
Pengcheng Wang ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Signaling Pathway ◽  
Wistar Rats ◽  
Cholesterol Metabolism ◽  
Expression Profiles ◽  
Receptor Interaction ◽  
Pathophysiological Mechanism ◽  
Rna Seq ◽  
Diaphragmatic Dysfunction ◽  
Controlled Mechanical Ventilation

Abstract Background Ventilator-induced diaphragmatic dysfunction (VIDD) is associated with weaning difficulties, intensive care unit hospitalization (ICU), infant mortality, and poor long-term clinical outcomes. The expression patterns of long noncoding RNAs (lncRNAs) and mRNAs in the diaphragm in a rat controlled mechanical ventilation (CMV) model, however, remain to be investigated. Results The diaphragms of five male Wistar rats in a CMV group and five control Wistar rats were used to explore lncRNA and mRNA expression profiles by RNA-sequencing (RNA-seq). Muscle force measurements and immunofluorescence (IF) staining were used to verify the successful establishment of the CMV model. A total of 906 differentially expressed (DE) lncRNAs and 2,139 DE mRNAs were found in the CMV group. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to determine the biological functions or pathways of these DE mRNAs. Our results revealed that these DE mRNAs were related mainly related to complement and coagulation cascades, the PPAR signaling pathway, cholesterol metabolism, cytokine-cytokine receptor interaction, and the AMPK signaling pathway. Some DE lncRNAs and DE mRNAs determined by RNA-seq were validated by quantitative real-time polymerase chain reaction (qRT-PCR), which exhibited trends similar to those observed by RNA-sEq. Co-expression network analysis indicated that three selected muscle atrophy-related mRNAs (Myog, Trim63, and Fbxo32) were coexpressed with relatively newly discovered DE lncRNAs. Conclusions This study provides a novel perspective on the molecular mechanism of DE lncRNAs and mRNAs in a CMV model, and indicates that the inflammatory signaling pathway and lipid metabolism may play important roles in the pathophysiological mechanism and progression of VIDD.

scholarly journals The clinical significance of glutathione peroxidase 2 in glioblastoma multiforme

2021 ◽  
Vol 12 (1) ◽  
pp. 032-039
Author(s):  
Bangming Guo ◽  
Wenjuan Liao ◽  
Shusheng Wang
Keyword(s):  
Glioblastoma Multiforme ◽  
Glutathione Peroxidase ◽  
Mrna Expression ◽  
Signaling Pathway ◽  
Clinical Significance ◽  
Cancer Cell ◽  
Statistical Significance ◽  
Adult Brain ◽  
Chemokine Signaling ◽  
Chemokine Signaling Pathway

Abstract Background Glioblastoma multiforme (GBM) is the leading cause of death among adult brain cancer patients. Glutathione peroxidase 2 (GPX2), as a factor in oxidative stress, plays an important role in carcinogenesis. However, its role in GBM has not been well established. The study aimed to investigate the clinical significance of GPX2 with GBM prognosis. Methods Data of GBM and healthy individuals were retrospectively collected from oncomine, cancer cell line encyclopedia (CCLE), gene expression profiling interactive analysis (GEPIA), UALCAN, and Human Protein Atlas. GPX2 mRNA expression was first assessed across various cancer types in oncomine and cancer cell lines from CCLE. The mRNA expression of GPX2 was compared between normal and GBM tissues using GEPIA (normal = 207; GBM = 163) and UALCAN (normal = 5; GBM = 156). The GPX2 methylation was analyzed using data from UALCAN (normal = 2; GBM = 140). The prognostic value of GPX2 in GBM was explored in GEPIA and UALCAN using Kaplan–Meier method. STRING database was used to construct protein–protein interaction (PPI) network and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. Statistical significance was set as <0.05. Results The current study revealed no significant differences in GPX2 expression between normal and GBM from GEPIA data (P > 0.05) and UALCAN (P = 0.257). Patients with higher GPX2 intended to have a poorer prognosis (P = 0.0089). The KEGG pathways found that chemokine-signaling pathway were the more preferred. Conclusions The findings demonstrated that GPX2 might be a potential diagnosis and prognostic indicator for GBM. Chemokine-signaling pathway may be involved in GPX2 function.

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